Normal T Lymphocyte Function in Patients with End-Stage Renal Disease Hemodialyzed with &amp;lsquo;High-Flux&amp;rsquo; Polysulfone Membranes

Degiannis, Dimitrios; Czarnecki, Margaret; Donati, D; Homer, Leroy; Eisinger, Robert P.; Raska, K; Rašková, Jana

doi:10.1159/000168120

Cited by 25 publications

(12 citation statements)

References 14 publications

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“…We found no changes in milogen-induced responses, which already before calcitriol therapy were normal. Hemodial ysis with cuprophane membranes have been shown to result in reduced mitogen-induced T-cell responses com pared to dialysis with 'high-flux' polysulfone membranes [24], Only 3 of our patients were dialyzed with cuphrophane membranes, which may explain the overall good mitogen-induced responses. The discrepancy in mitogeninduced responses between the study of Tabata et al [12] and ours is difficult to evaluate since neither the parame ters reflecting their patients' calcium/phosphorus metabo lism and l,25-(OH)2D} levels nor the type of dialysis membranes were given.…”

Section: Discussionmentioning

confidence: 68%

Intravenous Calcitriol Therapy Restores Reduced Antigen-Induced T-Lymphocyte Response in 1,25-(OH)2D3-Deficient Hemodialysis Patients

Antonen

Saha

Lagerstedt

et al. 1996

Nephron

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Ten hemodialysis patients were treated with intravenous calcitriol (1-1.5 μg 3 times per week) for 3 months and parameters reflecting cell-mediated immunity were measured before and at the end of treatment. Peripheral blood CD4+ cells increased from 33.1 ± 14.2 to 43.8 ± 5.8% (p < 0.05) causing a comparable increase in CD3+ cells (67.3 ± 14.3 vs. 77.1 ± 7.9%, p < 0.05), whereas CD8+cells did not change significantly (22.2 ± 5.4 vs. 25.5 ± 3.0%). Mitogen-induced lymphocyte stimulation responses were normal even before treatment and did not change. Antigen-induced T-cell responses were very heterogeneous before calcitriol therapy; those 5 with initially unmeasurably low serum 1,25-dihydroxyvitamin D₃ (1,25-(OH)₂D₃) had a weaker response than the other patients (3,873 ± 1,528 vs. 22,948 ± 13,684 cpm, p < 0.05). After calcitriol treatment the patients with pretherapy unmeasurably low serum 1,25-(OH)₂D₃ had a comparable response to other patients (16,220 ± 9,674 vs. 22,064 ± 10,331 cpm). Our study shows that calcitriol therapy restores the depressed antigen-induced T-cell response of the hemodialysis patients most deficient in 1,25-(OH)₂D₃.

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Section: Discussionmentioning

confidence: 68%

Intravenous Calcitriol Therapy Restores Reduced Antigen-Induced T-Lymphocyte Response in 1,25-(OH)2D3-Deficient Hemodialysis Patients

Antonen

Saha

Lagerstedt

et al. 1996

Nephron

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“…Comparing recent studies to those performed earlier in the 1980s, the mag nitude of the lymphopenia in HD patients is less striking [13], suggesting that improve ments in dialytic regimens or other aspects of dialysis patient care, such as better control of anemia with erythropoietin, may play a role. Some studies have suggested that frequent blood transfusions augment the lymphopenia of chronic renal failure [14],…”

Section: Lymphocyte Number and Phenotypementioning

confidence: 84%

“…This defect does not correct in patients hemodialyzed with cuprophane membranes al though one recent study suggests that the pro liferative response to high concentrations of PHA normalizes in those patients dialyzed with polysulfone membranes [13]. Abnormal PHA-induced proliferation does not necessar ily signify a T cell defect, since stimulation of proliferation by PHA requires intact accesso ry cell (monocyte/macrophage) function.…”

Section: Proliferation To Mitogensmentioning

confidence: 99%

T Cell Function in Chronic Renal Failure and Dialysis

Kelly¹

1994

Blood Purif

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This article briefly summarizes the literature regarding possible defects in cell-mediated immunity in the setting of chronic renal failure. It is difficult to precisely determine the proximate cause or level of such defects from most studies. Confounding variables include reports on mixed patient populations (predialytic chronic renal failure, hemodialysis patients, and peritoneal dialysis patients) and studies before and after the introduction of erythropoietin for end-stage renal disease patients. While it seems clear that lymphopenia, suboptimal responses to mitogens, abnormal cytokine gene expression, and abnormal IL-2R expression are seen in a number of dialysis patients, the role of uremia versus dialysis in producing these abnormalities is unclear. In addition, it is difficult to determine whether T cell abnormalities are primary or secondary to impaired function of other interacting immune cells, such as macrophages. Clinical implications of defects in cell-mediated immunity are additionally discussed.

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“…Since changes in im mune competence and lymphocyte functional responses of hemodialyzed patients may be affected by the dialysis membrane used [47], we studied this parameter also in the plasma of patients undergoing hemodialysis by means of cellulose acetate, polyacrylonitrile and polysulfone membranes. The results are summarized in figure 5.…”

Section: Plasma Level O F Soluble Il-2 Receptor In Hemodialysis Patientsmentioning

confidence: 99%

Immune Deficiency in Uremia: Interleukin-2 Production and Responsiveness and Interleukin-2 Receptor Expression and Release

Donati

Degiannis

Homer

et al. 1991

Nephron

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We have studied the role of interleukin-2 (IL-2) and its receptors in the impaired in vitro lymphocyte response characteristic of hemodialysis patients treated by means of cuprophane membranes. The proliferative response of T lymphocytes as well as T-cell-dependent B cell proliferation after stimulation with mitogens was significantly reduced in hemodialysis patients. The in vitro production of IL-2 after such stimulation in parallel cultures was found to be similar in patients and in controls. The expression of IL-2 receptor on the lymphocyte cellular membrane in the hemodialysis group was also similar to controls. The in vitro proliferative response of uremic lymphocytes to exogenous IL-2, however, was significantly depressed suggesting a reduced availability of biologically active IL-2 receptor. The release of soluble IL-2 receptor by lectin-stimulated lymphocytes in culture was also significantly lower in the patient group; yet, hemodialysis patients has a strikingly elevated level of plasma soluble IL-2 receptor, and similar high levels were also found in three other groups of end-stage renal disease patients dialyzed by means of cellulose acetate, polysulfone and polyacrylonitrile membranes, as well as in a group of uremic patients on conservative treatment. In the hemodialysis patient group a significant positive correlation between levels of soluble IL-2 receptor and the duration of hemodialysis was found. Since soluble IL-2 receptor has been reported to down-regulate lymphocyte responses, the elevation in plasma levels of soluble IL-2 receptor in hemodialysis patients may be a pathogenetic factor in the progressive development of impaired immunity associated with end-stage renal disease.

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Normal T Lymphocyte Function in Patients with End-Stage Renal Disease Hemodialyzed with ‘High-Flux’ Polysulfone Membranes

Cited by 25 publications

References 14 publications

Intravenous Calcitriol Therapy Restores Reduced Antigen-Induced T-Lymphocyte Response in 1,25-(OH)<sub>2</sub>D<sub>3</sub>-Deficient Hemodialysis Patients

Intravenous Calcitriol Therapy Restores Reduced Antigen-Induced T-Lymphocyte Response in 1,25-(OH)<sub>2</sub>D<sub>3</sub>-Deficient Hemodialysis Patients

T Cell Function in Chronic Renal Failure and Dialysis

Immune Deficiency in Uremia: Interleukin-2 Production and Responsiveness and Interleukin-2 Receptor Expression and Release

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